Animal Models: Illuminating the Pathogenesis of Sudden Infant Death Syndrome

摘要: Three research areas derived from human studies of epidemiology, pathology, and sleep in infants have made contributions to our understanding sudden infant death syndrome (SIDS). Epidemiological who died SIDS identified a variety risk factors associated with increased decreased (1-7), including prone sleeping position (8, 9), maternal cigarette smoking during pregnancy, heat stress the infant, often related overheated environments, excessive bed clothing, or other unsafe practices 10, 11). Additional include recent upper respiratory tract infection, sharing, prematurity, intrauterine and/or postnatal hypoxic stress.Similar progress origins has been by pathologists analysing brains were classified as SIDS. Analyses brain tissue these consistently revealed high prevalence abnormalities brainstem serotoninergic system an number serotonergic neurons, higher proportion neurons displaying immature morphology, levels serotonin (5-HT) its synthetic enzyme, tryptophan hydroxylase 2 (TPH2), 5-HT receptor binding intensity both nuclei themselves several that are important cardiorespiratory control (9, 12-16). Similar deficits described asphyxia (17). There persistent speculation suffered hypoxia (i.e. low oxygen levels) at some time preceding (18-22), appeared delay maturation (19-21, 23, 24).Finally, subsequently sequence repetitive episodes preceding, following, apnea bradycardia, followed autoresuscitative efforts restore normal breathing arouse (25-28). Death occurred when autoresuscitation arousal following prolonged failed regular adequate oxygenation. Many experienced sequences multiple apneic events which they recovered, only succumb final event failed.